Acute thrombosis in an aortic prosthesis: all mechanical valves are not the same.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to T Millane.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
OBJECTIVES: This study was conducted to assess whether myocardial ischemia and/or infarction are involved in the pathogenesis of late right ventricular dysfunction in adult survivors of atrial baffle repair for transposition of the great arteries in infancy. BACKGROUND: The medium-term success of intraatrial baffle repair for transposition of the great arteries is good, with many patients surviving into adult life, but prognosis can be limited by progressive right ventricular dysfunction. We hypothesized that ongoing myocardial ischemia and/or infarction are important factors in the pathogenesis of this complication. Radionuclide techniques offer an opportunity to study both myocardial perfusion and concomitant ventricular wall motion. METHODS: Dipyridamole sestamibi single-photon emission computed tomography followed by rest sestamibi single-photon emission computed tomography was used to assess right ventricular myocardial perfusion, wall motion, wall thickening and ejection fraction in 22 adolescents/young adults who had undergone atrial baffle repair for simple transposition of the great arteries at median 6.7 (range 0.5 to 54) months of age. The patients were aged 10 to 25 (median 15.5) years; 19 in New York Heart Association class I, 2 in class II and 1 in class III. All were in a regular cardiac rhythm during the studies. The right ventricular tomographic images were examined in three parallel and two orthogonal planes, analyzed in 12 segments. RESULTS: Perfusion defects were evident in all patients in at least one segment, in either the rest or stress images. Twelve patients (55%) demonstrated fixed defects only, nine (41%) had fixed and reversible defects and one (4.5%) had reversible defects only. Concomitant wall-thickening abnormalities occurred in 83% of segments with fixed perfusion defects, mirrored by a reduction in wall motion in 91% of segments analyzed. Right ventricular ejection fraction was correlated with age (R = 0.62; p = 0.002), and with wall-thickening abnormalities (R = 0.60; p < 0.005). CONCLUSIONS: Reversible and fixed perfusion defects with concordant regional wall motion abnormalities occur in the right (systemic) ventricle 10 to 20 years after Mustard repair for transposition of the great arteries; this may be important in the pathogenesis of late right ventricular dysfunction in this group.
The purpose of this randomized controlled study was to assess the haemodynamic effects, safety and tolerability in acute myocardial infarction (AMI) of one month of oral captopril, one month of oral isosorbide mononitrate and 24 h of intravenous magnesium. It was carried out in four United Kingdom and six Polish hospitals in consecutive phases: oral captopril vs oral mononitrate vs placebo were compared among 400 patients in a 'three-way' study; and then oral captopril vs placebo and oral mononitrate vs placebo were compared among 474 patients in '2 x 2' and '2 x 2 x 2' factorial studies (with 208 patients in the latter study also randomized between intravenous magnesium and open control). The factorial studies differed from the three-way study in that one group of patients was allocated both oral captopril and oral mononitrate, a higher maintenance dose of captopril was used (following the same initial dose), and once daily controlled-release mononitrate was used. In the three-way study, the mean of the lowest systolic blood pressures recorded during the first 4 h after randomization were (mmHg +/- standard error): 104 +/- 2 captopril vs 105 +/- 1 mononitrate vs 112 +/- 2 placebo (P < 0.001 for captopril or for mononitrate vs placebo), and in the factorial studies were 105 +/- 1 captopril vs 110 +/- 1 placebo (P < 0.01) and 106 +/- 1 mononitrate vs 108 +/- 1 placebo (NS). There was an excess of hypotension recorded among patients allocated active treatment (captopril > mononitrate > placebo) and there was a small, but significant, excess of cardiogenic shock with captopril compared with control in the factorial study. However, in these studies, neither captopril nor mononitrate were associated with any overall increase in the incidence of hypotension considered severe enough to lead to treatment being stopped. No other serious complications were observed, and compliance with study tablets at hospital discharge was not significantly different between the active and placebo groups. Patients allocated magnesium in the 2 x 2 x 2 factorial study had a slightly lower mean systolic blood pressure just after the initial 15 min bolus injection (126 +/- 2 magnesium vs 134 +/- 3 control; P < 0.05) but there were no significant differences during the subsequent 24 h maintenance infusion period. Apart from some facial flushing, magnesium did not appear to be associated with any complications.(ABSTRACT TRUNCATED AT 400 WORDS)
Magnesium deficit in man is very difficult to detect and even more difficult to study. However, a chance observation led to the investigation of cardiac transplant recipients as an in vivo model of drug-induced magnesium depletion. Clinical circumstances were such that the question of the correlation of serum and tissue magnesium levels might be addressed. Using the same model, investigation of myocardial calcium levels was undertaken. Significant myocardial magnesium depletion accompanied persistent hypomagnesaemia in over 50 per cent of cardiac transplant recipients. Repletion of myocardial magnesium occurred some weeks later than normalization of serum levels; these time lags may explain the lack of correlation of serum and tissue magnesium levels in these circumstances. Myocardial calcium levels were generally higher than expected from control studies, and were particularly high in magnesium-depleted subjects. These findings are keeping with those predicted from animal studies. Electrophysiological studies in the transplanted denervated heart are free of many of the confounding features of such studies in the native heart. Preliminary work involving pacing protocols designed to induce abnormalities of phase 4 of the action potential suggests that myocardial magnesium deficit does not produce a clinical arrhythmogenic substrate in the denervated heart. However, shortening of the effective ventricular refractory period in hypomagnesaemic patients was observed, and it was noted that concurrent hypokalaemia in this circumstance would be particularly disadvantageous. The data collected in the course of these studies is discussed, and mechanisms for the observed benefit of magnesium as a possible anti-ischaemic agent in the period following acute myocardial infarction are proposed.
Explore the source record for details and available documents.
Standard time domain variables from signal-averaged electrocardiography were examined in a population of 331 survivors of acute myocardial infarction. Of these subjects, 130 received early (less than 24 hours) thrombolytic therapy. During a follow-up of greater than or equal to 10 months, there were 17 arrhythmic events (8.5%) (sudden death or sustained symptomatic ventricular tachycardia) in the group without thrombolysis and 8 (6.2%) in those with thrombolysis. Statistically, highly significant differences between the signal-averaged electrocardiographic variables of patients with and without arrhythmic events were found in the group without thrombolysis, whereas only root-mean-square voltage of the terminal 40 ms of the signal-averaged QRS complex was statistically associated with outcome (the differences in the other 2 indexes being not significant) in patients with thrombolysis. When using 2 previously published categoric criteria for the diagnosis of abnormal signal-averaged electrocardiography, the performance of these criteria in predicting arrhythmic events was substantially better in the group without thrombolysis than in those with thrombolysis (positive predictive accuracy greater than 3 times lower). Retrospectively adjusted receiver-operator characteristics showed that for a sensitivity of 30%, the maximum achievable positive predictive accuracy of signal-averaged electrocardiography for arrhythmic events was 100% in the group without thrombolysis, but only 27% in those with thrombolysis. It is concluded that standard signal-averaged electrocardiography after acute myocardial infarction is less informative in patients who receive thrombolytic treatment.
Several studies indicate that the electrophysiologic substrate for sustained ventricular tachycardia differs from that of ventricular fibrillation. This prospective study examined whether there were clinically relevant differences between the predictive values of the standard time-domain signal-averaged (SA) electrocardiographic (ECG) variables for ventricular tachycardia and sudden death after myocardial infarction. Predischarge SA electrocardiograms were recorded in 332 patients after infarction. During a follow-up period of greater than or equal to 6 months, there were 12 sudden deaths (3.6%), 14 patients (4.2%) developed spontaneous sustained ventricular tachycardia and 20 patients (6%) died of circulatory failure. The sensitivity, specificity and positive predictive accuracy of the numerical values of the time-domain SA electrocardiographic variables for predicting sudden death and ventricular tachycardia were compared. The optimal criteria for predicting ventricular tachycardia required the positivity of greater than or equal to 2 of the standard time-domain SA variables, whereas the optimal criteria for predicting sudden death required the positivity of all 3 variables. A high specificity was sustained over a wider range of sensitivity for sudden death than it was for ventricular tachycardia and the values of the variables which provided the same sensitivity for sudden death and ventricular tachycardia were different. For a sensitivity of 70%, the positive predictive accuracy was 31% for predicting sudden death and 13% for predicting ventricular tachycardia. The study concludes that differences in the predictive characteristics of variables for ventricular tachycardia and sudden death may be used to refine postinfarction risk stratification.
This report describes a patient who developed acute severe exacerbation of mild rheumatic mitral regurgitation caused by ischemia in the territory of a small, non-dominant circumflex coronary artery without myocardial infarction.
The predictive characteristics of spectral temporal analysis and time domain analysis of the signal-averaged electrocardiogram (ECG) for postinfarction arrhythmic events were compared in 257 patients. During a 6-month follow-up period, 7 patients (2.7%) died suddenly and 9 (3.5%) developed spontaneous sustained ventricular tachycardia. The mean numeric values of the standard time domain signal-averaged ECG variables in patients without arrhythmic events differed significantly from those in patients with arrhythmic events. The mean values of the spectral temporal signal-averaged ECG variables did not differ between the two patient groups. A strategy requiring positivity in any two time domain signal-averaged ECG variables provided the optimal receiver operating characteristic curves for predicting arrhythmic events. With spectral temporal analysis, a strategy using the Hanning window and diagnosing a positive signal-averaged ECG when two variables were abnormal provided the optimal curve for predicting arrhythmic events. Receiver operating characteristic curves showed that over a wide range of sensitivity, time domain variables had higher specificity for predicting arrhythmic events than did spectral temporal variables. Time domain analysis also provided significantly fewer false positive results than did spectral temporal analysis up to sensitivity values of 70%. It is concluded that time domain analysis of the signal-averaged ECG is superior to spectral temporal analysis for predicting arrhythmic events after myocardial infarction.
AIMS: To examine the influence of age on the prediction of sudden death after acute myocardial infarction based on heart rate variability (HRv), left ventricular ejection fraction (LVEF), and the frequency of ventricular extrasystoles. BACKGROUND: Autonomic and left ventricular function and the frequency of ventricular extrasystoles change with age but the influence of age on the prediction of sudden death from these variables has not been examined. METHODS: The 477 patients who had been through an early postinfarction risk stratification protocol and followed up for a mean of 790 days were dichotomised at 60 years of age. RESULTS: Sudden deaths occurred with similar frequency in both age groups (12 (4.7%) of the 256 patients aged < 60 years and seven (3.2%) of the 221 older patients). Sudden death, however, accounted for 52% of all deaths in the young group but only 18.4% of all deaths in the older group (p < 0.01). An HRv index of < 20 units combined with an average of more than 10 ventricular extrasystoles an hour on Holter monitoring (VE10) had a sensitivity of 50%, a positive predictive accuracy of 33%, and a risk ratio of 18 in the young group (p < 0.001) but was not significantly predictive in older patients. The situation was similar when the combination of an LVEF < 40% with VE10 was considered. This combination had a sensitivity of 44%, positive predictive accuracy of 36.4%, and a risk ratio of 16.1 in young patients (p < 0.001), but was not significantly predictive in older patients. The combination of VE10 with either LVEF < 40% or HRv < 20 units gave a sensitivity of 75%, positive predictive accuracy of 30%, and a risk ratio of 30 in young patients (p < 0.001), but the relation between this combination and sudden death in older patients was not statistically significant. CONCLUSION: In postinfarction patients aged < 60 sudden death was a more predominant mode of death and was more reliably predicted from a depressed HRv index, an LVEF < 40%, and VE10 than in older postinfarction patients. These findings may have important implications for post-infarction risk stratification and management.
We developed a single-stage technique involving a proteolytic enzyme (pepsin) for the solubilization of cardiac muscle to measure magnesium in tissue. This new method has been developed specifically for use with very small cardiac biopsy samples (less than 1 mg) obtained with modern myocardial biopsy forceps. Pepsin digestion of the tissue releases magnesium ions into solution and, after centrifugation and dilution with lanthanum chloride, the resulting supernate is suitable for analysis by atomic absorption spectrometry. Recovery of magnesium after a single digestion approaches 99%. In direct comparison studies of pepsin digestion and a traditional method involving nitric acid extraction, the pepsin digestion consistently yielded more magnesium. In contrast to traditional methods of tissue solubilization, pepsin digestion is well suited to extraction of magnesium from the small biopsy samples commonly presented for analysis in clinical practice.
A 3-year-old girl presented with a febrile illness complicated by right ventricular outflow tract tachycardia, which persisted after resolution of the presumed viral infection. The tachycardia was intermittent, but was significantly exacerbated by exercise. Radiofrequency ablation (RFA) of the ectopic focus was successfully performed and the child remains free of tachycardia 12 months later. A review of the literature suggests that RFA in children is increasingly seen as a safe and convenient option for the treatment of supraventricular tachycardia, whereas the management of ectopic ventricular tachycardia in pediatric practice has not been well defined.
Explore the source record for details and available documents.
Intramitochondrial calcification has been reported in heart transplant recipients treated with high-dose cyclosporine. Myocardial magnesium depletion is common in this group and, on the basis of extensive data from animal studies, would be expected to produce similar mitochondrial deposition of calcium. This prospective study investigated the occurrence of such calcification in biopsy specimens obtained serially in nine heart transplant recipients with simultaneous analysis of myocardial magnesium. During a mean follow-up of 32 weeks, 24 biopsy specimens were analyzed from nine patients. Mitochondrial calcium deposition was more marked in biopsy specimens from recipients with magnesium depletion (p < 0.025). Early toxic cyclosporine levels occurred in three recipients associated with a significant but reversible increase in mitochondrial calcification (p < 0.0001). Histologic rejection and use of calcium antagonists did not modify these findings. It is concluded that although cyclosporine toxicity does induce mitochondrial calcium deposition, such deposition can occur in the absence of toxicity should myocardial magnesium depletion be concurrent. Long-term follow-up will establish the clinical sequelae of such observations. However, when taken together with the results of this study, recent reports of attenuation of accelerated graft atherosclerosis by calcium antagonists may suggest that cyclosporine-induced myocardial magnesium depletion may have an etiologic role in this multifactorial process.
OBJECTIVES: To shorten the stay in hospital of patients admitted with chest pain of uncertain origin, using clinical history and an unchanging ECG as a basis to inform patients on the post-take ward round of imminent discharge that same day (pending normal cardiac enzyme results), thereby facilitating actual discharge on the same day. DESIGN: A prospective observational study over a two-month period of consecutive patients admitted with chest pain of uncertain origin. SETTING: District general hospital in North-West England with a regional cardiothoracic centre on site. RESULTS: Of the 115 patients enrolled in the study (15% of acute medical admissions), 43 (37%) were identified by the investigators as likely to have normal cardiac enzymes and only one of them had evidence of important cardiac ischaemia (median actual length of stay, 3 days). The specificity of the protocol was 98%, with a sensitivity of 89%. CONCLUSIONS: A careful clinical history taken by experienced junior staff together with two sequential ECGs, can identify patients who may be discharged within 24 hours of admission with chest pain of uncertain origin. Significant bed savings would result from the instigation of this practice, with minimal requirement for extra resources.